A myocardial infarction results in a loss of contractile tissue with fibrous tissue replacement. Depending on the extent of the loss of myocardium, the increased functional demand imposed on the surviving myocardium may range from trivial to insurmountable. The individual with inadequately treated systemic hypertension and ventricular hypertrophy may have a qualitatively different response to a myocardial infarction than the normotensive individual since the remaining viable myocardium of the hypertensive is already sustaining an increased functional demand. To quantitate the relationship between the loss of myocardium and residual ventricular function, experimental myocardial infarctions will be produced in normotensive and genetically hypertensive rats. A well-healed, discrete infarct is produced in this rat model 21 days following coronary artery ligation. At this time baseline hemodynamics, maximum pumping and pressure generating ability of the intact left ventricle, and passive ventricular compliance will be assessed in infarcted and sham-operated normotensive and hypertensive rats. Various indices of ventricular performance will be related to myocardial infarct size as determined by planimetry of serial slices of left ventricle. Antihypertensive agents will be administered to normotensive and genetically hypertensive rats to determine whether arterial pressure reduction alters the relationship of infarct size and ventricular performance. It is hoped that these studies will provide a better understanding of the functional ability of the normal and hypertrophied heart to sustain and respond to a myocardial infarction.